Pathogenesis of Atherosclerosis
Erling Falk, MD, PhD*
Department of Cardiology, Aarhus University Hospital (Skejby), Aarhus, Denmark.
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Figure 1 Plaque heterogeneity within a given patient. (A) Cross section of a coronary artery cut just distal to a bifurcation. The atherosclerotic plaque to the left (circumflex branch) is fibrotic and partly calcified, whereas the plaque to the right (marginal branch) is lipid-rich with a nonoccluding thrombus superimposed. (B) Higher magnification of the plaque-thrombus interface reveals that the fibrous cap over the lipid-rich core is extremely thin, inflamed, and ruptured with a real defect—a gap—in the cap. Both arteries contain contrast medium injected postmortem. Trichrome stain, staining collagen blue and thrombus red.
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Figure 2 Average composition of advanced coronary plaque. Pie diagram illustrating the average composition of advanced atherosclerotic plaques (>75% stenosis by histology) in the coronary artery tree in fatal myocardial infarction (20). Hypocellular tissues (fibrosis, calcium, and necrosis) constitute by far the most voluminous plaque components.
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Figure 3 Molecular and structural targets for imaging. Cross section of a coronary artery containing plaque assumed to be rupture-prone. Potential targets for imaging are highlighted. They comprise: 1) the large lipid-rich necrotic core (orange asterisk), 2) thin fibrous cap (blue arrows), 3) expansive remodeling (green arrow), and 4) vasa vasorum and neovascularization (red open circles).
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